50-year old with chest pain, “no ischemic changes”

Written by Jesse McLaren

 

A previously healthy 50 year-old presented with 24 hours of intermittent exertional chest pain, radiating to the arms and associated with shortness of breath. It was ongoing on arrival in the emergency department. Below is the old ECG (on top) and then new ECG (on bottom). What do you think?

There is normal sinus rhythm, normal conduction, normal axis, and tall precordial voltages with J waves from early repolarization. The old ECG has proportional ST elevation and T waves. But the new ECG has new Q waves in aVL and V2 (the distribution of the first diagonal artery) – and in the next context of Q waves, the T wave in V2 is upright and relative large. In a previously healthy patient with new and ongoing chest pain, this is concerning for acute occlusion of the first diagonal artery.

Smith: Normal ST Elevation in V2-V4 never has an associated Q-wave!  So this STE cannot be considered normal even though there was STE on the previous ECG.

But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. The emergency physician was called to see the patient 90 minutes later after the troponin I returned at 1100 ng/L. This confirms these Q waves are caused by an acute infarct. But is the artery still occluded? 

 

The emergency physician noted the patient had improved but ongoing chest pain, and had the following repeat ECG:

Ongoing large T wave in V2 with ongoing symptoms = still an occluded artery. But the ECG still doesn’t meet STEMI criteria. It was therefore interpreted as “no STEMI” and the patient was treated with dual anti-platelets and referred to cardiology as “NSTEMI.”

 

Four hours after arrival cardiology saw the patient, with a repeat troponin that rose to 1900 ng/L. The patient was now painfree after anti-platelets and first two ECGs were interpreted as “no ischemic changes”. So they were admitted as “NSTEMI” with a plan to repeat troponin levels every 6 hours and perform angiography in 24-48 hours.

 

Was there spontaneous reperfusion? This would require resolution of chest pain and reperfusion on ECG, but would still be at risk for reocclusion. But no repeat ECG was done after symptom resolution. Eight hours after arrival the patient complained of recurring pain, with troponin now at 5,200 ng/L, and was treated with a nitro patch. This is concerning for reocclusion, but there was no repeat ECG and no change in the plan to wait for angiography. 

 

The next ECG was done 21 hours after arrival, after troponin peaked at 7400ng/L and then declined to 7000. This ECG was recorded when the patient was painfree:

Now we see reperfusion T wave inversion in aVL and V2, consistent with spontaneous reperfusion in a patient who was painfree. But the biphasic T waves in V2 are not “Wellens T waves” because they are preceded by acute Q waves and already a large infarct by troponin. This again confirms there is a critical lesion in the first diagonal, which is either transiently open or is still occluded but being perfused through collateral circulation. 

 

But there were no more ECGs for the next 8 hours before angiogram, and no further troponin levels for the remainder of the patient’s admission.

 

Angiogram found a totally occluded first diagonal artery, consistent with all the ECGs, which reperfused after stenting.

Smith: the ECG and troponin suggest reperfusion but the artery remains fully occluded.  This is usually a result of restoration of flow from collaterals.  This still image of the angiogram is not adequate to comment on collateral flow.

Next day the patient was discharged with a diagnosis of “NSTEMI” despite a totally occluded artery, and unknown peak troponin. Fortunately the periodic spontaneous reperfusion before the angiogram prevented the infarct from being much larger, and allowed the R wave to reconstitute on the discharge ECG (a final reminder that the initial Q wave was acute).

In summary, this patient’s occlusion was missed by

1.     the computer interpretation

2.     the emergency physician who signed off the ECG

3.     the treating emergency physician

4.     the cardiologist

5.     and worst of all, the discharge diagnosis that did not change despite an angiogram showing a 100% occlusion. This is not unusual but standard of care under the STEMI paradigm, where discharge diagnoses change to highlight false positive STEMI but not false negative STEMI

I sent the baseline and presenting ECG to the Queen of Hearts, without benefit of any clinical information (other than pre-test likelihood on which it is trained), and without the benefit of comparing with the old ECGs:

 

So in isolation and without context the ECG is not diagnostic of OMI. But with comparison to prior (which could be incorporated into future versions of the Queen of Hearts) and applied to clinical context it is diagnostic.

 

 

Take home

1.     ECGs are a snapshot in time, should be compared to prior, and should be repeated if symptoms are ongoing (to look for occlusion) or resolved (to look for reperfusion)

2.     STEMI criteria is bad at differentiating between normal variant and acute coronary occlusion or reperfusion, and initial troponin levels don't differentiate between occlusive and non-occlusive MI

3.     the presence of J waves from early repolarization doesn’t rule out an acute coronary occlusion

4.     Q waves can be acute and can resolve with reperfusion

5.     T waves require context: the same size T wave can be proportional to a normal QRS, or disproportionate relative to small QRS or Q wave

6.     Spontaneous reperfusion is still a high risk state, and can have a totally occluded artery on angiogram

7.     The diagnosis of NSTEMI misses OMI in real time, and does not change retrospectively to highlight false negative STEMI

8.     QOH can make expert OMI interpretation widely available 

 

 

Here is another great example of Q-wave evolution that is missed:

Acute MI from LAD occlusion, or early repolarization?

This is clearly OMI but was not recognized

Then 70 minutes later:

New Q-waves, still not recognized.

These are easy for the Queen:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  

For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

References

1.     McLaren et al, including Meyers/Smith. Missing occlusions: quality gaps for ED patients with occlusion MI. Am J Emerg Med 2023 

2.     Herman, Meyers, Smith et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Dig Health 2023

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MY Comment, by KEN GRAUER, MD (12/30/2023):

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Superbly documented case by Dr. McLaren — in which the unfortunate details of opportunities missed are sequentially recounted.

• Given the answers provided by cardiac catheterization — I thought review of the first 3 tracings in today's case especially insightful. For clarity and to facilitate comparison in Figure-1 — I've put these initial 3 tracings together.

Figure-1: I've put the first 3 ECGs in today's case together.

MY Thoughts on the first 3 ECGs in Today's Case:

Based on the first 2 ECGs in today's case ( = the initial ED tracing — and comparison with an "old" ECG on this patient) — Dr. McLaren correctly predicted acute OMI of the 1st Diagonal Branch of the LAD. I fully acknowledge that — I did not predict the "culprit" vessel until much later in today's course.

• We have previously shown many cases involving acute OMI of the 1st or 2nd Diagonal Branch of the LAD. These case are most readily recognizable by the South African Flag distribution of ST-T wave deviation (ie, ST elevation in leads I, aVL and V2 — with reciprocal ST depression in lead III — and no ST elevation in chest leads other than V2 — as detailed in the May 11, 2022 post by Dr. McLaren and myself). 
• 
  
• KEY Point: This typical pattern of D1 or D2 OMI is masked in today's tracing because of a "baseline" ECG ( = ECG #2 in Figure-1) that shows: i) Marked QRS increased amplitude in the lateral chest leads (R waves in leads V4,V5,V6 all exceeding 20 mm); ii) Early transition (Transition already by lead V2 in ECG #2, with R wave height exceeding S wave depth); — and, iii) A baseline repolarization variant, with 1-2 mm of J-point ST elevation in multiple leads. Given these findings on the "old" ECG — it would seem difficult to rapidly evolve an acute tracing with the poor R wave and ST elevation isolated to lead V2 that one would expect with acute D1 or D2 OMI.
• The "baseline" tracing in today's case already showed what I thought was a disproportionately large T wave by lead V2 (this T wave being taller than the R wave in lead V2 of ECG #2 — and much taller than the S wave in this lead is deep). That said — in the setting of J-point repolarization ST elevation and markedly increased R wave amplitudes beginning in neighboring lead V3 — I did not think anything in the "old" ECG looked acute. But I also did not perceive the T wave in lead V2 of ECG #1 to necessarily be abnormal in view of T wave appearance in lead V2 of ECG #2.
• 
  
• I perceived the fragmented QS in lead V2 of ECG #1 to clearly be of potential concern. That said, given isolation of this finding to lead V2 — I was not convinced this QS was real (and not the result of lead placement) — until I saw the identical-looking fragmented QS in lead V2 of ECG #3.

The Acute Findings I Focused on in ECG #1:

What convinced me of an acute ongoing cardiac event was comparison of the limb leads between the initial ECG in today's case and the "old" ECG:

• For me — the KEY lead in ECG #1 was lead aVL. Despite no significant change in frontal plane axis between ECGs #1 and #2 — there was no denying reduced T wave amplitude with beginning T wave inversion in ECG #1 compared to the "old" ECG (BLUE arrow in lead aVL of ECG #1).
• In view of this definite new change in lead aVL — there was no denying increased T wave amplitude in each of the inferior leads in ECG #1 compared to T wave appearance in the "old" ECG.
• 
  
• My Impression: Although I was uncertain about a "culprit" artery — in this patient with new and persistent CP — the indication for prompt cath was clear.

The 3rd ECG:

Movement artifact rendered interpretation of ECG #3 difficult in the limb leads. 

• KEY findings for me in ECG #3 included; i) The identical fragmented QS in lead V2 (that I thought confirmed the loss in R wave from lead V1 compared to the "old" ECG was a real and important finding); — and, ii) What I felt was a real and significant increase in T wave amplitude in lead V2 of ECG #3 compared to T wave amplitude in ECG #2 — consistent (as per Dr. McLaren) with 100% occlusion of D1, as found on cardiac catheterization. 

Acute OMI or "Benign" Early Repolarization?

Written by Willy Frick

A man in his 50s with a history of hypertension, dyslipidemia, type 2 diabetes mellitus, and prior inferior OMI status post DES to his proximal RCA 3 years prior presented to the emergency department at around 3 AM complaining of chest pain onset around 9 PM the evening prior. He described it as severe, sharp, and substernal with associated nausea, vomiting, chills, and diaphoresis. The following ECG was obtained. Note that the machine read is "normal sinus rhythm, normal ECG." Cardiology over read the tracing and signed the interpretation without modification.

ECG 1

What do you think?

The Queen of Hearts sees no OMI but only with low confidence. She seems concerned about a few leads.

I sent this ECG to Dr. Smith and Dr. Meyers with no clinical context. 

Dr. Smith said "That is a tough one. I would say OMI low confidence." 

Dr. Meyers noted the presence of South African Flag sign, indicative of high lateral OMI.

Smith comment: in clinical context, (middle aged with acute chest pain), the ECG is diagnostic and the cath lab should be activated.

The patient was given aspirin 324 mg PO, nitroglycerin 0.4 mg SL, and morphine 2 mg IV all simultaneously. Twenty minutes later, his pain was unchanged and he was given an additional dose of morphine 2 mg IV. Thirty minutes later he reported significant improvement in his chest pain. Cardiac troponin I drawn around that time resulted at 0.323 ng/mL (ref. <0.049 ng/mL).

Smith comment: this troponin alone should be enough data to activate the cath lab, regardless of the ECG.  

Also: As we always say, do not give morphine until you are committed to the cath lab.  The pain will resolve and you will think the ischemia is gone when it is only hidden!

Case continued: The hospitalist admission H&P an hour later describes 6/10 chest pressure, but also notes that he "has chest tenderness and upon palpation it reproduces his chest pain." This is classically taught as a strong argument for musculoskeletal etiology of pain. Note that as many as 7% of patients with acute coronary syndrome have chest pain reproducible on palpation [Lee, Solomon]. This equates to a negative likelihood ratio of 0.3, which reduces the pre-test probability of acute coronary syndrome by less than 30% [McGee].  

Smith comment: But the tests (ECG and troponin) are extremely specific and so the post test probability is nearly 100%.

Repeat cTnI drawn at around 8 AM was 3.910 ng/mL. Cardiology consult note written around that time documents that "Pain improved with NTG, morphine in ED but still present." (This patient was not one of the lucky 6.4% of patients taken for immediate heart catheterization due to uncontrolled chest pain [Lupu].) The note also says "slight lateral ST elevations noted, likely early repolarization since unchanged compared to 2014."

Brief aside: "Early repolarization" is a frequently proclaimed and poorly understood electrocardiographic phenomenon which mostly serves to reassure clinicians that not all ST elevations are ischemic (something readers of this blog know well). The original term "benign early repolarization" has fallen out of favor since the seminal paper by Haïssaguerre et al. linking the finding with long term risk of idiopathic ventricular fibrillation. The link is quite modest, increasing the chance of VF from 3.4 per 100,000 to 11 per 100,000 [Rosso].    

In an attempt to clarify language, a consensus definition was developed. The definition requires the following three components:

1. An end QRS notch (sometimes called a J wave) or slur, in the case of a slur it must lie entirely above the isoelectric baseline
2. The peak amplitude of the notch or slur should be ≥ 0.1 mV in 2 or more contiguous leads (excluding V1-V3)
3. The QRS duration should be < 120 ms

This definition is not perfect. It relies on an 1 mm cut point, which this blog does not favor as an approach to ECG. However, it does give us some context for thinking about benign causes of ST elevation.

Back to the case...

The patient's old ECG is shown below.

ECG 2

What do you think?

Compared to the presenting ECG, the Queen of Hearts sees no OMI with high confidence.

Notice that the old ECG does meet the consensus definition for early repolarization, but the current ECG does not. This is shown in the enlarged picture below.

It is therefore inaccurate to say that the ECG shows "unchanged" early repolarization. Here are the South African Flag Sign leads shown side by side, the older tracing on the left, the current tracing on the right.

                      Older tracing                                                  Current tracing

In lead I we see the disappearance (or marked diminution) of a previously prominent end QRS notch. In leads aVL and III, we see a change in ST segment morphology from markedly concave to much more angular. V2 has some changes, but at least to me it is not as clear what to make of them.

Fortunately, the patient was taken for heart catheterization that morning.

The first view shown below is right anterior oblique caudal. This view is usually best for visualizing the left circumflex and its branch vessels (called obtuse marginals).

Shown below is a still of the same view. Red indicates LAD, orange indicates ramus intermedius, yellow indicates LCx, and green indicates OM. In particular, the green OM arrow also points to a subtotal occlusion of the culprit vessel. You can see a barely visible thread of contrast connecting the proximal and distal portions of the OM right at the arrow head.

The next view shown below is the left anterior oblique caudal, also called the "spider view" which is best for visualizing the left main and proximal LAD, LCx, (and ramus intermedius, when present), as well as the proximal branch vessels, diagonal vessels off the LAD and obtuse marginals off the LCx.

Red indicates LAD, blue indicates diagonal, orange indicates ramus intermedius, yellow indicates LCx, and green indicates OM.

The next view shown below is the left anterior oblique cranial, which is best for visualizing the bifurcation between the LAD and the diagonal vessels.

Red indicates LAD, blue indicates diagonal, orange indicates ramus intermedius, yellow indicates LCx.

Finally, the next view shown is right anterior oblique cranial, which is best for visualizing most of the LAD (although it is not always great for the most proximal and distal portions).

Red indicates LAD, blue indicates diagonal, orange indicates ramus intermedius, yellow indicates LCx, and green indicates OM. In this view, the culprit lesion is not particularly obvious which is an important principle in angiography, and the reason why we obtain multiple views.

Just before 10 AM, the patient received a stent to the culprit OM. Peak troponin was 12 ng/mL. Before and after angiography is shown below. They are very slightly different angiographic views, the image on the left is right anterior oblique caudal, and the image on the right is more of an anteroposterior caudal (meaning no lateral angulation of the imaging).

You might be asking yourself: How does this qualifiy as OMI given that the culprit artery has TIMI 3 (meaning angiographically unimpaired) flow. Recall that approximately 20% of OMIs have TIMI 3 flow at angiography [Cox, Stone]. In this patient's case, there was also an ECG obtained the following morning, shown below.

Notice that there are now reperfusion T waves in I and aVL, confirming the diagnosis of OMI.

You might also be asking yourself why the ECG showed South African Flag sign given that the artery is more posterior than high lateral. The answer is probably that the proximal part of the artery is close to the high lateral position, and the distal part of the artery manifested extremely subtle posterior changes. Usually, posterior OMI manifests as anterior ST depression. The presenting ECG in this case did not show overt ST depression, but comparing to the old ECG, there is relative anterior ST depression. This is shown below side by side, old ECG on the left, new ECG on the right.

                                Old ECG                                     New ECG with acute chest pain

Learning points:

• Patients with early repolarization pattern are still at risk for OMI, and the underlying early repolarization pattern may obscure the presence of OMI.

• Chest pain reproducible on palpation does not rule out acute coronary syndrome. It reduces pre-test probability by less than 30%.

• "Normal" machine read does not rule out OMI.

• Posterior OMI may manifest as relative anterior ST depression without overt ST depression below the isoelectric baseline.

References:

Cox, D. A., Stone, G. W., Grines, C. L., Stuckey, T., Zimetbaum, P. J., Tcheng, J. E., Turco, M., Garcia, E., Guagliumi, G., Iwaoka, R. S., Mehran, R., O’Neill, W. W., Lansky, A. J., & Griffin, J. J. (2006). Comparative early and late outcomes after primary percutaneous coronary intervention in st-segment elevation and Non–St-segment elevation acute myocardial infarction (from the Cadillac trial). The American Journal of Cardiology, 98(3), 331–337. https://doi.org/10.1016/j.amjcard.2006.01.102

Lee, T. H., Cook, E. F., Weisberg, M., Sargent, R. K., Wilson, C., & Goldman, L. (1985). Acute chest pain in the emergency room. Archives of Internal Medicine, 145(1), 65. https://doi.org/10.1001/archinte.1985.00360010085013

Lupu, L., Taha, L., Banai, A., Shmueli, H., Borohovitz, A., Matetzky, S., Gabarin, M., Shuvy, M., Beigel, R., Orvin, K., Minha, S., Shacham, Y., Banai, S., Glikson, M., & Asher, E. (2022). Immediate and early percutaneous coronary intervention in very high‐risk and high‐risk non‐st segment elevation myocardial infarction patients. Clinical Cardiology, 45(4), 359–369. https://doi.org/10.1002/clc.23781

Macfarlane, P. W., Antzelevitch, C., Haissaguerre, M., Huikuri, H. V., Potse, M., Rosso, R., Sacher, F., Tikkanen, J. T., Wellens, H., & Yan, G.-X. (2015). The early repolarization pattern. Journal of the American College of Cardiology, 66(4), 470–477. https://doi.org/10.1016/j.jacc.2015.05.033

McGee, S. R. (2012). Chapter 27. In Evidence-based physical diagnosis. Elsevier/Saunders.

Rosso, R., Kogan, E., Belhassen, B., Rozovski, U., Scheinman, M. M., Zeltser, D., Halkin, A., Steinvil, A., Heller, K., Glikson, M., Katz, A., & Viskin, S. (2008). J-point elevation in survivors of primary ventricular fibrillation and matched control subjects. Journal of the American College of Cardiology, 52(15), 1231–1238. https://doi.org/10.1016/j.jacc.2008.07.010

Solomon, C. G., Lee, T. H., Cook, E. F., Weisberg, M. C., Brand, D. A., Rouan, G. W., & Goldman, L. (1989). Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients: The multicenter chest pain study experience. The American Journal of Cardiology, 63(12), 772–776. https://doi.org/10.1016/0002-9149(89)90040-4

Stone, G. W., Cox, D., Garcia, E., Brodie, B. R., Morice, M.-C., Griffin, J., Mattos, L., Lansky, A. J., O’Neill, W. W., & Grines, C. L. (2001). Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction. Circulation, 104(6), 636–641. https://doi.org/10.1161/hc3101.093701 

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MY Comment, by KEN GRAUER, MD (12/27/2023):

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Interesting case by Dr. Frick — with superb illustration by him of cardiac cath findings! In the interest of fostering discussion — I'll present my thoughts on the first 2 tracings in today's case, that include a slightly different perspective on certain features of this case.

• For clarity in Figure-1 — I've put these first 2 tracings together to facilitate comparison.

Figure-1: Comparison between the first 2 ECGs in today's case.

MY Thoughts on the ECGs in Figure-1:

In view of the history and the initial ECG in today's case — my thoughts and concerns were as follows:

• This patient is a 50s man with known coronary disease (s/p stenting of a previous inferior OMI) — who presented to the ED for severe CP (Chest Pain) of at least several hours duration, that was still ongoing at the time ECG #1 was obtained. As a result, even before looking at this patient's initial ECG — he falls into a high-prevalence likelihood group for ACS (for an Acute Coronary Syndrome). We therefore need to assume and rule "out" ACS — more than having to rule it "in". I did not see anything in ECG #1 that helped me to "rule out" OMI (= my opinion).
• We have discussed repolarization variants on multiple occasions in Dr. Smith's ECG Blog — with detailed description of this entity in the May 23, 2022 post by Dr. McLaren (Please check out My Comment and illustrative Figure at the bottom of the page of this post). For practical purposes — I favor the term, repolarization variant when doubt exists as to whether or not strict criteria for the newer definition of ER (Early Repolarization) are satisfied.
• Given the history in today's case — I was not in the least contemplating whether there was (or was not) some type of repolarization variant after seeing ECG #1. There clearly is slight-but-real ST elevation in leads I and aVL of this initial tracing — which places the "onus of proof" on us as medical providers to rule out ACS. 
• Finally (as per Dr. Frick) — mention is made of the hospitalist's notation of being swayed by the presence of chest tenderness "reproduced by palpation". While this physical exam finding may slightly increase likelihood of a musculoskeletal disorder — this is clearly a subjective finding associated with far-too-great of a false positivity rate to allow use in any meaningful way as a factor to rule out OMI. The "onus of proof" remains on us as medical providers to objectively rule out ACS.

My Concerns about ECG #1:

In addition to the slight-but-real ST elevation present in high-lateral leads I and aVL — I noted the following in ECG #1:

• Especially given the context of a patient with new CP — ST-T waves are not "normal" in any of the inferior leads. Instead — the ST segment is straighter-than-normal in both lead II and lead aVF (RED lines that I've drawn in these leads in Figure-1). It is easier to appreciate this subtle change in lead aVF than in lead II — but although loss of the gradual smooth upsloping of the ST segment in both of these leads (leading to a more abrupt junction between the end of the ST segment and the beginning of the T wave) is not diagnostic — it is also not "normal".
• Lead III is of more concern — as it shows the magical mirror-image opposite ST-T wave relationship with lead aVL that so often indicates acute inferior or high-lateral OMI (See My Comments regarding this "magical" mirror-image opposite relationship at the bottom of the page in the March 27, 2023 — the November 21, 2020 — the October 6, 2018 — and the July 11, 2018 posts — among many others).
• In the context of the above ECG changes in 5/6 of the limb leads — there is also suspicious (albeit non-diagnostic) ST segment straightening in lead V6 of ECG #1 (RED line in this lead).
• 
  
• BOTTOM Line: To emphasize that the above ECG changes in ECG #1 are non-diagnostic of an OMI — but in the context of a patient with known coronary disease who presents with persistent, severe CP — I interpreted these ECG changes as highly suspicious of possible OMI. As per Dr. Frick — even without any ECG changes, persistent ischemic-sounding CP is indication for prompt cardiac cath.

What about Lead V2 in ECG #1?

We have presented many cases in Dr. Smith's ECG Blog, in which suspicious but non-diagnostic limb lead ST-T wave changes are confirmed by ST-T wave abnormalities in leads V2 and/or V3 (in which we carefully attend to the slight, upward sloping ST elevation that is normally seen in these leads).

• As a result, after noting the above described abnormalities in the limb leads of ECG #1 — my "eyes" immediately focused on lead V2 — looking for any indication of "tell-tale" ST flattening or depression that might indicate posterior OMI, thereby confirming my suspicion of high-lateral OMI (by finding evidence of associated posterior OMI).
• Instead — lead V2 manifests an rSr' configuration with slight "saddleback" ST elevation. Rather than the South African Flag Sign — I thought the "extra" r' deflection that is not seen in the "old" ECG more likely suggested too-high placement of the lead V2 electrode. The shape of the ST elevation in lead V2 most commonly associated with a true S. African Flag Sign (due to acute OMI of D1 or D2) — is usually different than the gradual upsloping ST segment seen in the saddleback morphology of ECG #1. (See examples of OMIs with the S. African Flag Sign provided by Dr. McLaren — with additional detailed discussion of this entity in My Comment at the bottom of the page in the May 11, 2022 post in Dr. Smith's ECG Blog).
• In support of my suspicion that the "extra" r' in lead V2 of ECG #1 is the result of faulty placement of the lead V2 electrode — is the lack of any r' in the "old" ECG.
• NOTE: Although an rSr' deflect is seen in both leads V1 and V2 of the 3rd ECG done in today's case — the fairly deep negative component to the P wave in lead V1 of that tracing suggests too-high electrode placement of V1 and V2 in this final tracing done the next morning. (See My Comment in the April 17, 2022 post of Dr. Smith's ECG Blog for review of the 3 Clues to Too-High Placement of leads V1 and V2).
• 
  
• BOTTOM Line: I thought the ST-T wave appearance in lead V2 of ECG #1 likely represented a "technical misadventure" (due to too-high placement of the V2 electrode on the chest). Given the diagnostic importance of lead V2 (in assessing for postero-lateral OMI from LCx occlusion) — and — my suspected inability to accurately assess leaad V2 — I would have immediately repeated ECG #1 after verifying correct electrode lead placement.

What about the "Old" ECG?

In my opinion — the "old" ECG (that I've labeled ECG #2 in Figure-1) — does not provide an adequate tracing for us to compare with today's initial ECG:

• We are not told when, or under what circumstances ECG #2 was recorded. We know that today's patient has had prior inferior OMI with stenting of his proximal RCA ~3 years earlier. The relatively wide Q wave (qRS complex) in lead aVF of ECG #2, in association with deep (with respect to QRS amplitude) symmetric T wave inversion in leads III and aVF suggest that this "old" ECG may have represented reperfusion if it was obtained soon after the prior inferior OMI. Doubtless that more than a single ECG would have been obtained during that admission — without us knowing what the ultimate "stable" ECG pattern of this patient's "baseline" really is.
• The shape and relative size of ST-T wave changes in the inferior leads is quite different between ECG #1 and ECG #2 (I thought depth of the T wave inversion in lead III to be clearly disproportionate given its equal amplitude to the S wave in this lead).
• 
  
• BOTTOM Line: For prior tracings to be a valid source for comparison with a current tracing — we need to indicate clinical circumstances at the time the prior ECG was recorded (and ideally indicate if we know what the patient's true "baseline" ECG looks like).
• 
  
• P.S.: Given the concerns I raise above about the initial ECG in today's case — I would have expected at least several serial ECGs to be done — which had this been accomplished, could have prompted diagnostic (and therapeutic) cardiac cath much sooner than actually occurred.